title: Glucocorticoids in the management of systemic juvenile idiopathic arthritis.
abstract: Glucocorticoids have been the mainstay of treatment for many years in systemic-onset juvenile idiopathic arthritis (sJIA), causing important side effects and some difficulties in the management of this disease. Until the introduction of biologic agents, oral glucocorticoids were used to control fever and other systemic features for several months or even years if systemic manifestations persisted. Nowadays, clinicians have valid alternatives that have revolutionized the natural history of sJIA. Biologic agents, such as the interleukin-1 inhibitors anakinra and the more recent canakinumab, or the interleukin-6 inhibitor tocilizumab, have improved the prognosis of this debilitating disease. Glucocorticoids still have to be considered at the onset of disease when a non-steroidal anti-inflammatory drug therapy fails or when there are life-threatening complications such as severe anemia or pericarditis, or macrophage activation syndrome. Local (intra-articular) triamcinolone hexacetonide is the treatment of choice for arthritis limited to one joint or a few joints in patients without systemic activity. To date, there is still great heterogeneity in the management of sJIA patients, but in recent years there have been attempts to design algorithms and treatment protocols for glucocorticoids, disease-modifying anti-rheumatic drugs, and biologic agents. This review provides an overview of the current knowledge of glucocorticoid therapy in sJIA, comments on recently published recommendations, and gives practical support to the clinician for management of this disease.
authors.affiliation: Rheumatology Unit, AOU Meyer and University of Florence, V. le Pieraccini 24, 50141, Florence, Italy, gaia.vannucci@gmail.com.
authors.forename: Gaia
authors.initials: G
authors.lastname: Vannucci
authors.forename: Luca
authors.initials: L
authors.lastname: Cantarini
authors.forename: Teresa
authors.initials: T
authors.lastname: Giani
authors.forename: Edoardo
authors.initials: E
authors.lastname: Marrani
authors.forename: Davide
authors.initials: D
authors.lastname: Moretti
authors.forename: Ilaria
authors.initials: I
authors.lastname: Pagnini
authors.forename: Gabriele
authors.initials: G
authors.lastname: Simonini
authors.forename: Rolando
authors.initials: R
authors.lastname: Cimaz
mesh_terms: D000893:Anti-Inflammatory Agents / Q000009:adverse effects / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001171:Arthritis, Juvenile / Q000188:drug therapy*; D002648:Child; D005938:Glucocorticoids / Q000009:adverse effects / Q000627:therapeutic use*; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000627:therapeutic use; D007375:Interleukin-1 / Q000037:antagonists & inhibitors; D055501:Macrophage Activation Syndrome / Q000209:etiology / Q000517:prevention & control; D014221:Triamcinolone / Q000627:therapeutic use; D000093242:Interleukin-6 Inhibitors
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D005938:Glucocorticoids; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D014221:Triamcinolone; D000093242:Interleukin-6 Inhibitors; C541220:canakinumab; C502936:tocilizumab